“Our study demonstrates the high sensitivity of [gallium Ga-68 dotatate] in the localization of [ectopic Cushing’s syndrome], for both occult primary tumors and metastatic lesions,” the researchers wrote. “Importantly, the use of [gallium Ga-68 dotatate] impacted clinical management in 64% of patients with [ectopic Cushing’s syndrome] overall.” The researche […]

The 11th annual Pituitary Day will take place on October 19, 2019 Patients living with pituitary disorders can hear lectures from our pituitary specialists, see movies of pituitary surgeries and hear from other patients about their experience living with pituitary disease and undergoing surgery.

Cynthia is from Ruckersville, VA. She is testing for Cushing's due to many symptoms. tested for CD because after exhaustive research on AVN (Avascular Necrosis) related to other diseases. I have four known areas of AVN & after seeing the symptoms of CD, I realized may have this. I also have numerous other diseases Lupus, Sojgrens, Hypothyroid, High […]

Today is the Thirteenth Anniversary of my kidney cancer surgery. These thirteen years have been bonus years for me. For my cancer stage, the 5-year survival rate was 81% and I’ve made it more than twice that long – so far.

Kathy was diagnosed with a pituitary tumor in 1991. At the time the only symptom she was aware of was a severe headache. She had a transsphenoidal resection followed by radiation therapy for 23 days. They said they could not remove all of the tumor.

Sadly, we lost another Cushing’s patient on Friday, May 9, 2014. Melinda was a member of the Cushing’s Help message boards since Jun 24, 2007. She was only 25 and left behind a young son and many loving family members.

He died of a presumed heart attack. September 19, 2015 he said "'I was diagnosed hypertensive way back when I was 20. The condition remained for years, and became more acute with my cushings pit tumor. I still have high blood pressure, partially teated with three meds. I'll have to consult my doc and see if this may also be an issue."

'My name is Caroline and I dont post often but have met a few of you guys and read the board regularly, it has definitely been a godsend to cushies everywhere. The reason I am writing tonight is I have just received devastating information about a dear friend of mine, and a woman some of you may have met during testing. Her name is Kathryn Miller and sh […]

Patients with growth hormone deficiency due to nonfunctioning pituitary adenoma experienced excessive morbidity due to cerebral infarction and sepsis regardless of whether they received long-term GH therapy, whereas treatment was associated with a normal incidence of type 2 diabetes, despite higher BMI and more severe hypopituitarism in treated patients, according to findings from an observational, registry-based study.

“Although growth hormone replacement therapy is well-established and reverses most of the features associated with GH [deficiency], one of the safety concerns is the reduction in insulin sensitivity and the potential risk of developing type 2 diabetes mellitus,” Daniel S. Olsson, MSc, MD, PhD, professor at the Sahlgrenska Academy Institute of Medicine at the University of Gothenburg, Sweden, and colleagues wrote in the study background.

Studies examining whether there is an association have produced mixed results, the researchers wrote, and it remains unknown to what extent GH deficiency — and GH therapy —contribute to the development of type 2 diabetes and other comorbidities, including cerebral infarction, malignant tumors, myocardial infarction or fractures.

Olsson and colleagues analyzed data from 426 patients treated or followed for nonfunctioning pituitary adenoma between 1997 and 2011, selected from the Swedish National Patient Register. Researchers assessed information on tumor treatment, hormone therapy, antihypertensive medication, BMI and duration of GH therapy. For patients with type 2 diabetes, researchers assessed HbA1c values, insulin treatment, oral antidiabetes therapies and lipid-lowering therapies. Researchers followed the cohort through December 2014 or until death. Patients were stratified by use of GH therapy. Researchers calculated standardized incidence ratios (SIRs) based on the observed number of comorbidities among patients with nonfunctioning pituitary adenoma vs. the expected number of comorbidities in the background population.

Within the cohort, 207 patients received GH therapy (145 men) and 219 did not (129 men). Median duration of GH therapy was 11.7 years; mean age at diagnosis was 56 years for treated patients and 65 years for untreated patients. Median follow-up time for treated and untreated patients was 12.2 years and 8.2 years, respectively.

Incidence of cerebral infarction was increased for the whole cohort regardless of GH therapy status, with an SIR of 1.39 (95% CI, 1.03-1.84), and was most evident among 97 patients who underwent radiotherapy, in which 19 cerebral infarctions occurred vs. the expected number of 9.8 (P = .011).

“The study showed an increased overall incidence of cerebral infarction in patients with [nonfunctioning pituitary adenoma] compared to the general population that was related to previous radiotherapy, but not to GH [replacement therapy],” the researchers wrote.

Incidence of myocardial infarction was similar for treated and untreated patients, with SIRs of 1.18 (95% CI, 0.73-1.8) and 1.23 (95% CI, 0.82-1.78), respectively. Incidence of receiving medical treatment for hypertension was also similar between groups.

In assessing incidence of type 2 diabetes, the researchers found that the SIR was higher among untreated patients (1.65; 95% CI, 1.06-2.46) vs. treated patients, who had an SIR similar to the background population (0.99; 95% CI, 0.55-1.63). Treated patients with type 2 diabetes had higher BMI vs. untreated patients with type 2 diabetes (P = .01), according to researchers, and glycemic status was similar among treated and untreated patients.

The incidence of sepsis requiring hospitalization was also similar between treated and untreated patients, with rates for both groups close to double that of the background population (P < .001). Incidence of malignant tumors was not increased for treated or untreated patients when compared against the background population, according to the researchers. – by Regina Schaffer

Disclosures: The Gothenburg Growth Hormone Database is supported partly through unrestricted grants from Novo Nordisk, Pfizer and Sandoz. Olsson reports he has served as a consultant for Ipsen, Pfizer and Sandoz. Another author reports he has served as a consultant to AstraZeneca and Viropharma/Shire, and received lecture fees from Novo Nordisk, Otsuka and Pfizer.

Although excessive weight gain is a common symptom of Cushing’s disease, existing indications advise clinicians to test for Cushing’s in obese people only if the disease is clinically suspected.

The utility of measuring LNSC for Cushing’s disease screening is well established. However, differences in assays, sample collection methods, and controls have led to a great variability in the proposed reference ranges and cut-off values. Also, according to the Endocrine Society, the influence of gender, age, and co-existing medical conditions on LNSC concentrations is still unclear.

Regarding obesity, data on the specificity of assessing late-night salivary cortisol levels is contradictory, as some studies found no differences while others reported lower specificity compared to healthy individuals.

An additional factor complicating LNSC measures in obese people is the prevalence of type 2 diabetes mellitus (T2DM), which may also lead to elevated cortisol levels.

Research showed a high rate of false-positive LNSC measurements in obese patients with poorly controlled type 2 diabetes. Also, in patients with recently diagnosed diabetes, investigators found that LNSC had very low specificity — the proportion of patients with Cushing’s who test positive — and a poor predictive value.

Recent reports showed a high diagnostic accuracy using automated electrochemiluminescent assays (ECLIA) in patients with Cushing’s disease. These methods use special labels conjugated to antibodies that produce light when they bind to a specific target.

The research team used an ECLIA assay to test the specificity of LNSC in obese patients both with and without diabetes. The investigators also intended to establish a reference range and cut-off value for this diagnostic approach.

Adults who requested weight loss treatment were included in the study, including 34 patients with a confirmed diagnosis of Cushing’s and 83 obese people, defined as having a body mass index (BMI) of at least 35 kg/m2. Forty healthy individuals were also analyzed.

Eight out of the 34 Cushing’s patients had a BMI within the obese range, which correlates with an overlap in patients awaiting bariatric surgery for weight loss, the investigators observed.

Compared to healthy and obese participants, measuring LNSC in Cushing’s disease patients had a maximum sensitivity of 67.6% and a specificity of 85.4%. This was lower than prior data from obese patients with two features of Cushing’s disease.

The cut-off value for detecting Cushing’s was 12.3 nmol/L, which is in line with other studies “and underlines the importance of an evaluation with an obese cohort vs. [Cushing’s disease],” the investigators wrote.

Results did not show an association between BMI, type 2 diabetes, and LNSC for all groups.

“In our obese cohort, we found that LNSC assayed by ECLIA had a low specificity in the diagnosis of [Cushing’s disease],” the researchers wrote. “However, the clear advantage of LNSC over other tests is the simple and stress-free sampling method.”

Traditionally, exams of patients with glucocorticoid excess focused on the presence of changes in anabolism (the chemical synthesis of molecules). Given the increase in obesity in the general population, changes in anabolism can no longer distinguish Cushing’s syndrome from metabolic syndrome.

However, analyses of anti-anabolic changes of cortisol – including osteopenia (lower bone density), thin skin, and ecchymoses (injury that causes subcutaneous bleeding) – are an effective way to make this distinction.

The worldwide prevalence of metabolic syndrome in obese people is estimated at about 10%. Conversely, the incidence of undiagnosed Cushing’s syndrome is about 75 cases per 1 million people.

Cushing’s and metabolic syndrome share significant clinical similarities, including obesity, hypertension, and type 2 diabetes. Therefore, “making the diagnosis is the least certain aspect in the care of patients with [Cushing’s],” Loriaux wrote.

Regarding a physical examination, patients with osteoporosis, reduced skin thickness in the middle finger, and three or more ecchymoses larger than 1 cm in diameter and not associated with trauma are more likely to have Cushing’s. Researchers estimate the probability of people with all three of these symptoms having Cushing’s syndrome is 95%.

Measuring 24-hour urinary-free cortisol levels allows the assessment of excess glucocorticoid effects, typical of Cushing’s syndrome. The test, which should be done with the most stringent techniques available, averages the augmented secretion of cortisol in the morning and the diminished secretion in the afternoon and at night.

Dexamethasone suppression is one of the currently used screening tests for Cushing’s syndrome. Patients with obesity and depression should not show decreased plasma cortisol levels when dexamethasone is suppressed. However, given its low estimated predictive value (the proportion of positive results that are “true positives”), “this test should not influence what the physician does next and should no longer be used” to screen for Cushing’s, the author wrote.

Some patients may show evidence of Cushing’s syndrome at a physical examination, but low urinary free cortisol excretion. This may be due to glucocorticoids being administered to the patient. In this case, the glucocorticoid must be identified and discontinued. Periodic Cushing’s assessments that measure urinary free cortisol should be performed.

The opposite can also occur: no clinical symptoms of Cushing’s, but elevated urinary free cortisol excretion and detectable plasma levels of the hormone corticotropin. In these patients, the source of corticotropin secretion, which can be a tumor or the syndrome of generalized glucocorticoid resistance, must be determined.

The disease process can be corticotropin-dependent or independent, depending on whether the hormone is detectable. Corticotropin in Cushing’s syndrome can come from the pituitary gland (eutopic) or elsewhere in the body (ectopic).

Loriaux recommends that the source of corticotropin secretion be determined before considering surgery. Up to 40% of patients with pituitary adenomas have nonfunctioning tumors (the tumor does not produce any hormones) and the corticotropin source is elsewhere. If misdiagnosed, patients will likely undergo an unnecessary surgery, with a mortality rate of 1%.

Patients with an ectopic source of corticotropin should undergo imaging studies in the chest, followed by abdominal and pelvic organs. If these tests fail to detect the source, patients should undergo either the blockade of cortisol synthesis or an adrenalectomy (removal of adrenal glands).

However, corticotropin-independent Cushing’s is usually caused by a benign adrenal tumor that uniquely secretes cortisol.

“Such tumors can be treated successfully with laparoscopic adrenalectomy,” Loriaux wrote. If the tumor secretes more than one hormone, it is likely malignant. Surgical to remove the tumor and any detectable metastases should be conducted.

Overall, “the treatment for all causes of [Cushing’s syndrome], other than exogenous glucocorticoids, is surgical, and neurosurgeons, endocrine surgeons, and cancer surgeons are needed,” Loriaux wrote in the study.

“This level of multidisciplinary medical expertise is usually found only at academic medical centers. Thus, most, if not all, patients with [Cushing’s syndrome] should be referred to such a center for treatment.”

Cushing’s sydnrome [sic]: Condition can have the same symptoms as high blood pressure

The condition is a hormonal disorder caused by prolonged exposure to the hormone cortisol – which can be caused by taking steroids. Cortisol regulates metabolism and immune response in the body.

Other people develop Cushing’s syndrome because their bodies produce too much cortisol.

It is most common in adults aged between 20 and 50 although women are almost three time [sic] as likely to be diagnosed.

While the condition is rare and only affects around one in every 50,000 people – the syndrome can affect people with type 2 diabetes, obese and have poorly controlled blood sugar levels.

The condition is also more common in people with high blood pressure.

Cushing’s syndrome – also called hypercortisolism – can cause a number of symptoms.These can include:Weight gainThinning skin which can bruise easilyReddish-purple stretch marks on the arms, legs, breasts, thighs, stomach and buttocksIt can also cause the face to become rounder – causing fat to deposit on the faceMuscle or bone weakness is also a sign of the conditionA loss of libido – decreased interest in sex – is also a symptom

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Cushing’s sydnrome [sic]: Condition has similar symptoms as high blood pressure and metabolic syndrome

However, other symptoms can include excess hair on the face, irregular periods, severe fatigue, high blood pressure, high blood sugar irritability or depression and even a fatty deposit between the shoulders.The National Institute of Diabetes and Digestive and Kidney Diseases said: “Metabolic syndrome – a combination of problems that includes excess weight around the waist, high blood pressure, abnormal levels of cholesterol and triglycerides in the blood, and insulin resistance-also mimics the symptoms of Cushing’s syndrome.”Cushing’s syndrome often develops as a side effect of treatment with corticosteroids.

Corticosteroids are widely used to reduce inflammation and treat autoimmune conditions – where the immune system malfunctions and attacks healthy tissue – such as rheumatoid arthritis, Crohn’s disease and lupus.

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Cushing’s sydnrome [sic]: Condition can have the same symptoms as high blood pressure

Metabolic syndrome also mimics the symptoms of Cushing’s syndrome

However, the condition can be hard to diagnose because of the similarity to high blood pressure.To diagnose the disease, patients will usually need to have a saliva test, urine test and blood test to measure cortisol levels in the body.To treat the condition, patients will usually have to decrease the levels of steroids they are taking.

However, there are complications if the condition is left untreated.

It can lead to high blood pressure and increase the risk of heart disease and stroke.

In adults with adrenal incidentaloma, adiponectin levels may help predict the presence of subclinical Cushing’s disease, according to recent findings.

Asli Dogruk Unal, MD, of the department of endocrinology and metabolism at Memorial Atasehir Hospital in Istanbul, and colleagues analyzed data from 40 patients with adrenal incidentaloma (24 women; mean age, 61 years) and 30 metabolically healthy adults without adrenal adenomas or hyperplasia (22 women; mean age, 26 years). All patients with type 2 diabetes were newly diagnosed and not on any antidiabetic therapies; included patients were not using statin therapy for about 12 weeks.

In two group comparisons, researchers found that only adiponectin level was lower in the subclinical Cushing’s syndrome group vs. the nonfunctional adrenal incidentaloma group (P = .007); there were no observed between-group differences for age, BMI, waist circumference, insulin levels, homeostasis model assessment for insulin resistance (HOMA-IR) or lipid profiles.

Adiponectin level was negatively associated with insulin level, HOMA-IR, triglyceride level and midnight cortisol level, and was positively associated with body fat percentage, HDL and adrenocorticotropic hormone levels. In linear regression analysis, age was found to be an increasing factor, whereas sex, HOMA-IR, LDL, waist circumference and presence of subclinical Cushing’s syndrome were decreasing factors.

In evaluating the receiver operating characteristic analysis, researchers found that adiponectin level had a predictive value in determining the presence of subclinical Cushing’s syndrome (area under the curve: 0.81; 95% CI, 0.67-0.96). Sensitivity and specificity for an adiponectin value of 13 ng/mL or less in predicting the presence of subclinical Cushing’s syndrome were 87.5% and 77.4%, respectively; positive predictive value and negative predictive value were 50% and 96%, respectively.

“Presence of [subclinical Cushing’s syndrome] should be considered in case of an adiponectin level of 13 ng/mL in [adrenal incidentaloma] patients,” the researchers wrote. “Low adiponectin levels in [subclinical Cushing’s syndrome] patients may be important in treatment decision due to the known relation between adiponectin and cardiovascular events. In order to increase the evidences on this subject, further prospective follow-up studies with larger number of subjects are needed.” – by Regina Schaffer